Oncolytic viruses such as rodent parvoviruses represent novel tools for cancer treatment [1, 2]. Besides specifically killing cancer cells (oncolysis), these agents also provide danger signals prompting the immune system to eliminate virus-infected tumors [3]. As a consequence of oncolytic events, the innate and adaptive immune systems gain access to tumor antigens, which may result in cross-priming and vaccination effects [4, 5]. Rodent parvoviruses are single-stranded DNA viruses possessing “intrinsic” oncolytic activity, i.e. they preferentially replicate in and kill cancer cells of both murine and human origin [6, 7]. Yet the anticancer efficacy of the most promising candidates for human clinical applications (including H-1PV) needs to be improved. So far, for improvement the following strategies were applied:
(a) Creation of PV-based vectors by introducing therapeutic genes (e.g., chemokines or cytokines)[8, 9, 10];
(b) Use of natural rodent PVs in combination with chemotherapeutic drugs (e.g., gemcitabine)[11]; and
(c) Creation of PV mutants bearing point mutations at potential phosphorylation sites of the large non-structural protein NS1 [12].
However, the results obtained need further improvement, in particular as regards higher anti-tumor potential compared to natural PVs currently used, and reduction of time during the production step.